This application proposes to study the development of normal human rod function. The rods transduce light into an electrical signal and so initiate vision. Immaturities of rod phototransduction processes may explain more of the immaturities of human scotopic vision than previously recognized. The applicant discusses evidence that, compared to adults', infants' rod outer segments are shorter and the concentration of rhodopsin is lower in the discs of the outer segment. The evidence leads to predictions that both the saturated (maximum) amplitude and amplification (or gain) of the rod photoresponse will increase with development, but the rate of developmental increase will be slower for amplification. Additionally, the delayed anatomic maturation of rods at the posterior pole, an area amounting to 5% to 10% of the total retinal area, is considered, and predicted to account for differential courses of development of posterior pole vs peripheral sensitivities; posterior pole sensitivity is expected to increase more slowly. Studies of electroretinographic (ERG) a-waves and psychophysical thresholds in young infants and adult control subjects, and rhodopsin will be used to test these hypotheses. Post receptoral components (b-wave; scotopic threshold response) of the ERG will evaluate the development of the flow of rod mediated information across the retina. These experiments will generate new knowledge that will advance our understanding of the development of normal, human visual capacities. When this information is applied to future pediatric patients, it is expected to disclose mechanisms of rod cell disease and so contribute to the design of novel therapeutic strategies.